This project has confirmed previous reports of deficient PMN chemotaxis in juvenile periodontitis. Attempts at determining the metabolic basis for the functional inadequacy have begun. Evidence has been obtained for the possibility of a cAMP metabolic difference between "normal" and those exhibiting defective chemotactic responsiveness. We have demonstrated a disassociation between PMN chemeotaxis and lysosomal enzyme release (N-acetyl-Beta-D-glucosaminidase) in PMN from persons with juvenile periodontitis. Using pharmacological probes to manipulate cAMP levels intracellularly, we are studying the reversibility of the chemotaxis defect in vitro, and the effect on enzyme release, in further pursuit of the metabolic site of the defect.